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Hyperkapnie — Symptom oder protektive Strategie?

  • Conference paper
Nasale Maskenbeatmung im Kindes- und Erwachsenenalter

Summary

Chronic respiratory failure (CRF) is caused by a decrease in the capacity of the respiratory muscles (e. g., neuromuscular diseases) or an increase in load (e. g., kyphoscoliosis or obstructive lung disease) or both. CRF is characterized by hypercapnia and hypoxemia. The degree of hypercapnia is directly related to the increase of the load and decrease of the capacity of the respiratory muscles and acts therefore as an indicator.

Are there strategies of the respiratory muscles which serve to protect themselves from fatal fatigue? From the teleological point of view one could create a hypothesis based on the typical change of breathing patterns in patients with CRF. For example, the increased load due to the compromised lung and chest wall mechanics in patients with severe kyphoscoliosis by a chronic increase of energy consumption leads to energy depletion in the respiratory muscles. As a protective strategy, the work of breathing is decreased below the threshold of respiratory muscle failure via the reduction of tidal volume and minute ventilation, respectively. Simultaneously, the increased breathing frequency compensates for the reduced tidal volume in order to guarantee the neccessary minute ventilation. However, the simultaneous decrease of the alveolar ventilation due to an increased dead space is associated with a reduced gas exchange characterized by hypoxemia and hypercapnia. The respiratory center adapts to the limited capacities of the respiratory muscles, adjusting its output in a way that the work of respiratory muscles will not exceed the muscle fatigue level. Accordingly, the sensitivity of the CO2 chemoreceptors must be blunted in order to avoid an increase of the breathing drive and to reach a „permissible hypercapnia“.In this hypothesis secondary hypoventilation and hypercapnia, respectively, may be viewed as an intelligent compensating mechanism to the reduced capacity of the respiratory muscles or increase in load. Furthermore, slowly developing hypoxemia and hypercapnia are compensated by cellular and circulatory adaptation mechanisms.

Vorabdruck mit freundlicher Genegmigung des Steinkopff Verlags.Aus: Intensivmedizin (1997); (erweiterte Fassung des Vortrags auf der Tagung „Nichtinvasive nasale Maskenbeatmung — Brücke zur Lungentransplantation?“ 14./15.11.1996 in Dresden)

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Literatur

  1. Aida A, Miyamoto K, Nishimura M, Kawakami Y, Aiba M, Kira S (1994) Effect of hypercapnia on survival of patients with long-term oxygen therapy: Comparison between patients with COPD and sequelae of pulmonary tuberculosis. Am J Respir Crit Care Med 149: A183

    Google Scholar 

  2. Albelda SM, Gefter WB, Kelley MA, Epstein DM, Miller WT (1983) Ventilator-induced subpleural air cysts: clinical, radiographic, and pathologic significance. Am Rev Respir Dis 127: 360–365

    PubMed  CAS  Google Scholar 

  3. Bégin P, Grassino A (1991) Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. Am Rev Respir Dis 143:905–912

    PubMed  Google Scholar 

  4. Blackburn JP, Conway CM, Leigh JM, Lindop MJ, Reitan JA, (1972) PaCO2 and the preejection period; the PaCO2/inotropy response curve. Anesthesiology 37: 268–276

    Article  PubMed  CAS  Google Scholar 

  5. Boekstegers P, Weiss M (1990) Tissue oxygen partial pressure distribution within the human skeletal muscle during hypercapnia. Adv Exp Med Biol 277: 525–531

    PubMed  CAS  Google Scholar 

  6. Chailleux E, Fauroux B, Binet F, Dautzenberg B, Polu JM (1996) Predictors of survival in patients receiving domociliary oxygen therapy or mechanical ventilation. 109: 741–749.

    CAS  Google Scholar 

  7. Cohen Y, Chang LH, Litt L, Kim Fm Severinghaus JW, Weinstein PR Davis Rl, Germano i, James TL (1990) Stability of brain intracellular lactate and 3iP-metabolite levels at reduce intracellular pG during prolonged hypercapnia in rats. J Cereb Blood Flow Metab 10: 277–284

    Article  PubMed  CAS  Google Scholar 

  8. Cooper CB, Waterhouse J, Howard P (1987) Twelve year clinical study of patients with hypoxic cor pulmonale given long term domociliary oxygen therapy. Thorax 42: 105–110

    Article  PubMed  CAS  Google Scholar 

  9. Covelli HD, Black JW, Olsen MS, Beekman JF (1981) Respiratory failure precipitated by high carbohydrate loads. Ann Intern Med 95: 579–581

    PubMed  CAS  Google Scholar 

  10. Criée CP (1988) Analysis of inspiratory mouth pressures. Prax Klin Pneumol 42: 820–826

    PubMed  Google Scholar 

  11. Darioli A, Perret C (1984) Mechanical controlled hypoventilation in status asthmaticus. Am Rev Respir Dis 129: 385–387

    PubMed  CAS  Google Scholar 

  12. Dreyfuss D, Soler P, Basset G, Saumon G (1988) High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume and positive end-expiratory pressure. Am Rev Respir Dis 137: 1159–1164

    PubMed  CAS  Google Scholar 

  13. Dripps RD, Comroe JH (1947) The respiratory and circulatory response of normal man to inhalation of 7.6 and 10.4 percent CO2 with a comparison of the maximal ventilation produced by severe muscle exercise, inhalation of CO2 and maximal voluntary hyperventilation. Am J Physiol 149: 43–51

    PubMed  CAS  Google Scholar 

  14. Dubois P, Jamart J, Machiels J, Smeets F, Lulling J (1994) Prognosis of severely hypoxemic patients receiving long-term oxygen therapy. Chest 105: 469–474

    Article  PubMed  CAS  Google Scholar 

  15. Edvinsson L, McKenzie ET,, Mc Culloch J (1993) Cerebral blood flow and metabolism. Chap.4. 2: Changes in arterial gas tension. New York: Raven Press: 524–552

    Google Scholar 

  16. Eiser N, Denman WT, West C, Luce P (1991) Oral diamorphine: lack of effects on dyspnoea and exercise tolerance in the “pink puffer” syndrome. Eur Respir J 4: 926–931

    PubMed  CAS  Google Scholar 

  17. Feihl F, Perret C (1994) Permissive hypercapnia. Am J Respir Crit Care Med 150: 1722–1737

    PubMed  CAS  Google Scholar 

  18. Glauser FL, Fairman RP, Bechard D (1987) The causes and evaluation of chronic hypercapnea. Chest 91: 755–759

    PubMed  CAS  Google Scholar 

  19. Goldstein B, Shannon DC, Tordes ID (1990) Supercarbia in children: Clinical course and outcome. Crit Care Med 18: 166–168

    Article  PubMed  CAS  Google Scholar 

  20. Gomes Vianna L, Koulouris N, Lanigan C, Moxham J (1990) Effect of acute hypercapnia on limb muscle contractility in humans. J Appl Physiol 69: 1486–1493

    Google Scholar 

  21. Gores GJ, Nieminen AL, Fleishman KE, Dawson TL, Herman B, Lemasters JJ (1988) Extracellular acidosis delays onset of cell death in ATP-depleted hepatocytes. Am J Physiol 255: C315–322

    PubMed  CAS  Google Scholar 

  22. Graham GR, Hill DW, Nunn JF (1960) Die Wirkung hoher CO2-Konzentrationen auf Kreislauf und Atmung. Toleranz und “Supercarbie”. Der Anaesthesist 9:70–73

    Google Scholar 

  23. Guilleminault C, McQuitty J, Ariagno RL, Challamel MJ, Korobkin R, McClead RE (1982) Congenital central alveolar hypoventilation syndrome in six infants. Pediatrics 70 (5): 684–694

    PubMed  CAS  Google Scholar 

  24. Hickling KG, Henderson SJ, Jackson R (1990) Low mortality associated with low volume, pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med 16: 372–377

    Article  PubMed  CAS  Google Scholar 

  25. Juan G, Calverley P, Talamo C, Schnader J, Roussos C (1984) Effects of carbon dioxide on diaphragmatic function in human beings. N Engl J Med 310: 874–879

    Article  PubMed  CAS  Google Scholar 

  26. Kacmarek RM, Hickling KG (1993) Permissive hypercapnia. Respir Care 38: 373–38

    Google Scholar 

  27. Kellogg RH (1964) Central chemical regulation of respiration. In: Fenn WO, Rahn H, eds. Handbook of physiology: respiratory (vol 1, sec 3 ). Washington, DC: American Physiological Society: 507–534

    Google Scholar 

  28. Kiely DG, Cargill IC, Lipworth J (1996) Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans Chest 109: 1215–1221

    CAS  Google Scholar 

  29. Köhler D, Criee CP, Raschke F (1997) Leitlinien zur hauslichen Sauerstoff- und Heimbeatmungs therapie. Med Klin 92: 2–6

    Article  Google Scholar 

  30. Kolobow T, Moretti MP, Fumagalli R, Mascheroni D, Prato P (1987) Severe impairment of lung function induces by high peak airway pressure during mechanical ventilation. Am Rev Respir Dis 135: 312–315

    PubMed  CAS  Google Scholar 

  31. Laier-Groeneveld G (1993) Richtlinien zur Indikation und Durchfülirung der intermittierenden Selbstbeatmung (ISB). Med Klinik 88: 509–510

    CAS  Google Scholar 

  32. Lanier WL, Weglinski MR (1991) Intracranial pressure. In: Cucchiara FF, Michenfelder JD, eds. Clinical neuroanesthesia. New York: Churchill Livingstone: 77–110

    Google Scholar 

  33. Litt L, Gonzales-Mendez R, Severinghous JW, Hamilton WK, Shuleshko J, Murphy-Boesch J, James TL (1985) Cerebral intracellular changes during supercarbia: an in vivo 31P nuclear magnetic resonance study in rats. J Cereb Blodd Flow Metab 5: 537–544

    Article  CAS  Google Scholar 

  34. Loftus CM, Silvidí JA, Bernstein DD, Kosier T (1989) Effects of hypercapnia on cerebral blood flow following prophylactic and delayed experimental superficial temporal artery-middle cerebral artery bypass. Surg Neurol 31: 183–189

    Article  PubMed  CAS  Google Scholar 

  35. Medical Research Council Working Party (1981) Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1: 681–686

    Google Scholar 

  36. Meissner HH, Franklin C (1992) Extreme hypercapnia in a fully alert patient. Chest 102: 1298–1299

    Article  PubMed  CAS  Google Scholar 

  37. Miller JD (1987) Cerbral blood flow variations with perfusion pressure and metabolism. In: Wood JH, ed. Cerebral blood flow. Physiologic and clinical aspects. New York: McGraw-Hill: 119–130

    Google Scholar 

  38. Neff TA, Petty TL (1972) Tolerance and survival in severe chronic hypercapnia. Arch Intern Med 129: 591–596

    Article  PubMed  CAS  Google Scholar 

  39. Paljärvi L, Söderfeldt B, Kalimo H, Olsson Y, Sieströ B (1982) The brain in extreme respiratory acidosis. A light and electron-microscopic study in the rat. Acta Neuropathol (Berl) 58: 87–94

    Article  Google Scholar 

  40. Petrozzino, JJ, Scardella AT, Edelman NH, Santiago TV (1993) Respiratory muscle acidosis stimulates endogenous opioids during inspiratory loading. Am. Rev. Respir. Dis. 147: 607–615

    PubMed  CAS  Google Scholar 

  41. Petty TL (1987) CO2 can be good for you! Respir Management 4: 65–66

    Google Scholar 

  42. Potkin RT, Swenson ER (1992) Resuscitation from acute severe hypercapnia. Determinants of tolerance and survival. Chest 102: 1742–1745

    Article  PubMed  CAS  Google Scholar 

  43. Prys-Roberts C. Hypercapnia (1980) In: Gray TC, Nunn JF, Utting JE, eds. General anaesthesia, 4th ed. London: Butterworth & Co: 435–460

    Google Scholar 

  44. Prys-Roberts C, Kelman GR, Greenbaum R, Robinson RH (1967) Circulatory influences of artificial ventilation during nitrous oxide anaesthesia in man. II: Results: The relative influence of mean intrathoracic pressure and arterial carbon diaoxide tension. Br J Anaesth 39: 533–548

    Article  PubMed  CAS  Google Scholar 

  45. Prys-Roberts C, Kelman GR, Greenbaum R, Robinson RH (1968) Hemodynamic and alveolar-arte-rial PO2 differences at varying PaCO2 in anaesthetized man. J Appl Physiol 25: 80–87

    Article  PubMed  CAS  Google Scholar 

  46. Prys-Roberts C, Smith WDA, Nunn JF (1967) Accidental severe hypercapnia during anaesthesia. Br J Anaesth 39: 257–267

    Article  PubMed  CAS  Google Scholar 

  47. Rebuck AS, Slutsky AS (1981) Measurement of ventilatory responses to hypercapnia and hypoxia. In: Hornbein TF, ed. Regulation of breathing: part II. New York: Marcel Dekker: 745–772

    Google Scholar 

  48. Rochester DF (1988) Does respiratory muscle rest relieve fatigue or incipient fatigue? Am Rev Respir Dis 138: 516–517

    PubMed  CAS  Google Scholar 

  49. Rochester DF (1991) Respiratory muscle weakness, pattern of breathing, and CO2 retention in chronic obstructive pulmonary disease. Am Rev Respir Dis 143: 901–903

    PubMed  CAS  Google Scholar 

  50. Schönhofer B, Ardes P, Geibel M, Köhler D, Jones P (1997) Evaluation of a movement detector to measure daily activity in patients with chronic lung diasease (aktuell eingereicht )

    Google Scholar 

  51. Schönhofer B, Köhler D (1994) Ventilatorische Insuffizienz und hyperkapnische Kompensation infolge chronisch belasteter „Atempumpe“. Dtsch med Wschr 119: 1209–1214

    Article  PubMed  Google Scholar 

  52. Sechzer PH, Egbart LD, Linde HW, Cooper DY, Dripps RD, Price HL (1960) Effects of CO2 inhalation on arterial pressure, ECG and plasma catecholamines and 17-OH corticosteroids in normal man. J Appl Physiol 15: 454–458

    PubMed  CAS  Google Scholar 

  53. Siesjö BK, Folbergrova J, MacMilian V (1972) The effect of hypercapnia upon intracellular pH in the brain, evaluated by the becarbonate-carbonic acid method and from the creatine phospokinase equilibrium. J Neurochem 19: 2483–2495.

    Article  PubMed  Google Scholar 

  54. Ström K, Boman G (1993) Long-term oxygen therapy in parenchymal lung diseases: an analysis of survival. Eur Respir J 6: 1264–1270

    PubMed  Google Scholar 

  55. Tang WC, Weil MH, Gazmuri RJ, Bisera J, Rackow EC (1991) Reversible impairment of myocardial contractility due to hypercarbic acidosis in the isolated perfused rat heart. Crit Care Med 19: 218– 224

    Google Scholar 

  56. Tuxen DV (1994) Permissive hypercapnia ventilation. Am J Respir Crit Care Med 150: 870–874

    PubMed  CAS  Google Scholar 

  57. Viitanen A, Salmenperä M, Heinonen J (1990) Right ventricular response to hypercapnia after cardiac surgery. Anaesthesiology 73: 393–400

    Article  CAS  Google Scholar 

  58. Vitacca M, Foglio K, Scalvini S, Marangoni S, Quadri A, Ambrosino N (1992) Time course of pulmomary function before admission into ICU. 102: 1737–1741

    CAS  Google Scholar 

  59. Walley K, Lewis TH, Wood LDH (1990) Acute respiratory acidosis decreases left ventricular contractibility but increases cardiac output in dogs. Circ Res 67: 628–635

    PubMed  CAS  Google Scholar 

  60. Weinberger SE, Schwarzstein RM, Weiss JW (1989) Hypercapnia. N Engl J Med 321: 1223–1231

    Article  CAS  Google Scholar 

  61. West JB (1971) Causes of carbon dioxide retention in lung diseases. N Engl J Med 284: 1232–1236

    Article  PubMed  CAS  Google Scholar 

  62. Wexels JC, Myhre ES (1987) Hypocapnia and hypercapnia in the dog: effects on myocardial blood flow and haemodynamics during beta- and combined alpha- and beta-adrenoreceptor blockade. Clin Physiol 7: 21–33

    Article  PubMed  CAS  Google Scholar 

  63. Xu Y, Cohen Y, Litt L, Chang LH, James TL (1991) Tolerance of low cerbral intracellular pH in rats during hyperbaric hypercapnia. Stroke 22: 1303–1308

    Article  PubMed  CAS  Google Scholar 

  64. Young IH, Daviskas E, Keena VA (1989) Effects of low dose nebulised morphine on exercise endurance in patients with chronic lung disease. Thorax 44: 387–390

    Article  PubMed  CAS  Google Scholar 

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Authors
  1. B. Schönhofer
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Editors and Affiliations

  1. Klinik und Poliklinik für Kinderheilkunde, Technische Universität Dresden Universitätsklinikum Carl Gustav Carus, Fetscherstraße 74, D-01307, Dresden, Germany

    E. Paditz

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Schönhofer, B. (1997). Hyperkapnie — Symptom oder protektive Strategie?. In: Paditz, E. (eds) Nasale Maskenbeatmung im Kindes- und Erwachsenenalter. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60853-7_11

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  • DOI: https://doi.org/10.1007/978-3-642-60853-7_11

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-63154-5

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